Acute Pulmonary Edema of Altitude
Clinical and Physiologic Observations
FRED, M.D., ALEXANDER M. SCHMIDT, M.D.,
TALCOTT BATES, M.D., AND HANS H. HECHT, M.D.
By HERBERT
L.
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A N ACUTE, RAPIDLY progressive, and
,tAx sometimes fatal illness characterized by
pulmonary edema occasionally idevelops in
apparently healthy mountaineers climbing at
high altitudes.1 This condition has received
renewed attention lately because of its possible relation to an illness occurring in some
natives of high altitude who develop acute
pulmonary edema upon returning from brief
sojourns to sea level.2 The pathogenesis and
mechanism of these forms of "acute pulmonary edema of altitude" are unclear.1-6 In
the past, either the victims died in high mountain regions before help arrived or the available medical facilities were not suitable for
accurate physiologic measurements. We recently had the opportunity to observe in
detail two physicians who developed this syndrome while skiing at high altitudes. The
results of these investigations form the basis
of this report.
Case Reports
Case 1
T.B., a 48-year-old physician, an experienced
skier and mountain climber, considered himself
in good health when he arrived at Alta, Utah,
(altitude 8,500 feet-2,600 M.) early on the
morning of March 26, 1961, after an overnight
trip by train from his home at sea level. He
skied vigorously for 2 days in heavy spring snow
at altitudes between 8,500 and 10,300 feet (2,600
to 3,125 M.).
During the evening of the second day of
skiing, he experienced dyspnea and a nonproductive cough. By next morning dyspnea and
cough had become more distressing, and he now
also noted nausea, vertigo, and generalized headFrom the Department of Medicine, University of
Utah College of Medicine, Salt Lake City, Utah.
Supported in part by a grant from the Utah
Heart Association and by U. S. Public Health Service
grant HTS-5150.
Circulation, Volume XXV, June 1962
929
ache. There was no orthopnea. Codeine sulfate,
15 mg., and aspirin, 600 mg., taken orally every
3 to 5 hours, partially controlled the cough and
headache. At noon, he began to vomit each time
he attempted to eat or drink. Severe paroxysms
of unproductive cough occurred with any change
of position and with the effort required to drink.
Repeated auscultation of the chest by a physician
companion demonstrated only coarse rales following episodes of cough. The patient suffered a restless night, afraid to move lest he precipitate
paroxysms of coughing.
On the morning of the third day, the patient
was barely able to speak because of extreme
dyspnea. His cough had become productive of
frothy sputum and was present almost constantly.
The pulse measured 120 beats per minute, the
respirations were 50 per minute. He preferred
to lie in the supine position partially rotated to
the right side. He had had no chills, fever, or nasal
discharge. Because of rapid deterioration in his
condition, he was taken by car to Salt Lake City
(altitude 4,200 feet-1,275 M.). He noted some
reduction in dyspnea during the descent.
The patient had diphtheria at age 4, and
poliomyelitis at age 36 without significant residual.
He had always been a vigorous, active individual
and had skied several times this winter, but only
at altitudes between 3,900 and 8,000 feet (1,200
to 2,400 M.). There was no history of pulmonary
or cardiovascular disease. It is of considerable
interest that his father, always in vigorous health,
died at the age of 43 while mountain climbing
near Cuzco, Peru, (altitude 11,200 feet-3,400
M.) 2 days after a 24-hour ascent from sea level.
Dyspnea, weakness, prostration, and coma preceded his death.
At the time of admission the patient appeared
moribund. He was apprehensive, breathless, and
eyanotic. He had a weak voice and an intermittent
cough productive of frothy clear sputum. The
temperature was 99 F. (orally), pulse 110 beats
per minute, respirations 38 per min-ute, blood
pressure 130/90 mm. Hg. The hands were cold
and clammy, and fingernails, toenails, and lips
were cyanotic. The neck veins were not distended.
The heart size was normal by percussion but a
presystolic gallop rhythm was heard in the xiphoid
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Serial roentyenoqrams of the chest
region and over the apex. The seconid heart sounid
over the pulmonic area was split throughout the
respiratory cycle. No mlurmurs were heard. Mediuin rales were present in the basilar portions of
the lower lobe of each lung. The remainder of
the physical examination was not remarkable.
The laboratory data were as follows: the volumne
of packed red cells was 51 mnl./100 -nl., the
white blood cell count was 9,800m/In.3, with
2 per cent juveniles, 72 per cent neutrophils, 20
per cent lynmphocytes, and 6 per cenit monocytes.
The icterus index was 5 and the erythrocyte
sedimentation rate was 8 mmi./hr. (Wintrobe).
The stool guaiac test and serologic test for syphilis
(VDRL) were negative. Urinalysis was normal.
The blood urea nitrogen, fasting blood sugar,
Fit st e psocXe.
seran chloride, and three serumn glutamic oxaloacetic transaminase determiniations all were w.ithin normal limits. The venous pressure was 16.0
cmn. of saline, and the circulation time (arm- to
tongue), with 5 ml. of sodium decholate, was
14 seconds. On admnission the electrocardiogram
showed only sinus tachyeardia. A phonocardiogram
confirmed the observed splitting of the pulmonic
second sound. On later occasions electrocardiograms and phonocardiogranis were entirely normial. On the fourth hospital dax, the venous
pressure was 6.0 cm. of saline, the circulation
time was 11 seconds, and the volume of packed
red cells was 44 ml./100 ml. The white blood cell
count and urinalysis remained normal.
Roentgenograms of the chest were taken serially.
Circulation. Volume XXV, June 1962
ACUTE PULMONARY EDEMA OF ALTITUDE
931
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rigure 2
Euarlg increase in the parenchymal lesions in patient TI. B. First episode
Table 1
Aacte Pulmonary Edema of Altitude (T.B., Age 48, Male)
Gross spirometry
Measured
VC (liters)
MBC (liters/mninute)
MMF (liters/second)
3rd day illness
March 30, 1961
After recovery
May 15, 1961
4.5
123
1.32
5.2
140
5.6
Predicted"2
4.0 -+" 0.8
120 ± 24
4.4 ± 2.2
VC, vital capacity; MBC, maximum breathing capacity; MMF, maximum mid-expiratory
flow.
The first of these showed a normal cardiac contour and bilateral pulmonary infiltrates (fig. 1).
The second roentgenogrami taken 4 hours after
admission showed a distinct increase in pulm-ionary
infiltration even though the patienit had improved
by this time (fig. 2). Subsequent films showed
gradual clearing. A normiial lung field was seen
on April 3, 1961 (fig. 1).
The results of g ross spiromietry performed on
the second hospital da-y wvere normal except for
a moderate reduction in inaximiumt midexpiratory
flow rate. Spirometry following recovery was
entirely normiial (table 1).
Cardiac catheterization was carried out on the
day after admission while the patient was still
quite ill. Cardiac output was estimated with
use of arterial and pulhuonary artery oxygen
content for the analyses as well as a venous
Circulation, Volume XXV, June 1962
injection of Indocyanine Green with direct arterial
sampling through a Wood oximeter. Pressures
were obtained by means of two Statham P23 Db
strain gages. The findings are listed in tables
2 and 3, and demonstrated: (a) modest arterial
hemoglobin desaturation that was not completely
corrected by inhalation of 100 per cent oxygen;
(b) elevation of pulnonary artery pressure that
decreased significantly during 100 per cent oxygen
breathing; and (e) normal left atrial and pulmonary vein pressures. The latter pressures were
obtained by advancing the catheter through a
probe-patent foramen ovale into the left atrium
and thence into a pulmonary vein. These positions
were verified by obtaining highly oxygenated
blood from both sites: pulmonary vein, 16.0 vols.
per cent-89 per cent saturation; left atrium,
15 vols. per cent-84 per cent saturation. These
FRED, SCHMIDT, BATES, HECHT
932
Table 2
Acute Pulmonary Edema of Altitude: Catheterization Data
T.B. age 48, male;
Het: 46%
height: 72 in.
Hgb: 14.2 Gm./100 ml.
S.A.: 1.95 M.2
weight: 163 lbs.
R.Q.: 0.87, supine, resting
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(A) Gas analysis: (a) Blood
pH: 7.38 units
Oxygen capacity of Hgb: 18.4 Vols. %
On 100% 02 inhalation: 17.8
CaO2 (Vol. %0) 14.0
76
on 100%o 02 inhalation: 97
SaO2 (%)
PaCO2 (mm. Hg) 32
CaCO2 (Vol. %) 42.5
Cv 02 (Vol. %) 9.3
(b) Lungs
V02 (ml./min.) 260
VE (L./min./M.> 5.9
(B) Flow estimates:
4.6
CI (L./min./M.Y) 2.9 (Oxygen-Fick)
CO (L./min.)
3.0 (Indoeyanine Green)
2.8 (Indoeyanine on 100% (O2)
Stroke volume (ml./beat) 57
CaO2, oxygen content of arterial blood; SaO2, oxygen saturation of hemoglobin of arterial
blood; CiY02, oxygen content of mixed venous blood; CaCO2, carbon dioxide content of arterial
blood; CO, cardiac output; CT, cardiac index; PaCO2, partial pressure of carbon dioxide
in arterial blood; V:E;, minute ventilation; V02, oxygen consumption per minute.
Table 3
Acute Pulmonary Edema of Altitude: Vascular Pressures (in mm. Hg), Supine
Room air
T.B. age 48, male
Right atrium
Left atrium
Right ventricle
Pulmonary artery
Pulmonary vein
Brachial artery
Pulrnonary vascular resistance/M.'
(clinical units)
*Obtained by planimetry.
Phasic
Mean*
10/5
9/3
64/7
68/39
12/7
124/83
13.8
8
6
values compared to 9.3 vols. per cent-50 per
cent saturation in the pulhonary artery, and were
higher than an arterial sample obtained at an
earlier time (oxygen content of arterial blood:
14.0 vols. per eent-saturation 76 per cent).
V lid pulmonary "wedge" pressures could not be
obtained, even though the catheter tip was repeatedly placed far out into the distal subpleural
branches of the pulmonary artery. In spite of
these attempts, only widely fluctuating pressures
of indistinct contour were recorded. An indicatordilution curve obtained by injecting 3 ml. of
Indocyanine Green into the pulmonary artery
and sampling from the brachial artery was of
normal configuration and displayed normal time
relations of its components. The ratio of the
disappearance time to the buildup time of the
curve was 1.8. This, together with the normial
100% 02 inhalation (7 min.)
Mean*
Phasic
46
44/27
10
100
129/87
34
104
10.0
pulmonary artery blood oxygen content suggested
the presence of a probe-patent foramen ovale
rather than a hemodynamically significant atrial
septal defect.
An extensive search for infection was negative.
Three routine cultures of the sputum grew normal
flora. A 24-hour collection of sputum was negative on culture for acid-fast and fungus organisms.
A blood culture was sterile. No virus was isolated
from tissue cultures of three throat washings and
three stool specimens. Serologic studies on acute
and convaleseent sera drawn 4 weeks apart were
negative with regard to brucella, tularemia, WeilFelix, heterophile antibody, typhoid, influenza A
and B, Q-fever, psittacosis, cold agglutinins, and
to ECHO, coxsackie, and adenoviruses. Skin tests
for tuberculosis were not applied because of a
history of strong reaction to tuberculin. HistoCirculation, Volume XXV, June
1962
ACUTE PULMONARY EDEMA OF ALTITUDE
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plasmin and coccidioidin skin tests were negative,
however, during the acute illness and 1 month
later.
The patient received oxygen by nasal catheter
shortly after his admission to the hospital. The
response to this therapy was dramatic. Within
15 minutes, the eyanosis and gallop rhythm disappeared, and the patient felt markedly improved.
When oxygen was discontinued, eyanosis and the
gallop rhythm promptly returned. During the
first 48 hours, the patient was treated only with
bed rest and intermittent administration of oxygen. On the third hospital day, the gallop rhythm
was absent permanently. By the fourth day the
pulmonic second sound was no longer split, and
the aortic second was louder than the pulmonic
second sound. The patient was discharged well,
5 days after admission.
The possibility of a recurrence of the illness
was discussed when it was learned that he had
previously planned a high mountain trip for the
forthcoming summer. Since similar patients have
tolerated re-exposure to high altitude,5 it was
decided that the trip could be attempted cautiously.
On July 12, 1961, the patient began a gradual
ascent into the Sierra Nevada Mountains of
California. During the fourth day on the trail,
camp was made at 8,400 feet (2,575 M.). Here
he noted diplopia and headache. Three days later
at an elevation of 10,200 feet (3,100 M.) severe
weakness and nausea occurred also. On the eighth
day of the hike, the patient reached an altitude
of 10,600 feet (3,200 M.). He awoke the next
morning with intense headache, weakness, and
severe nausea. He vomited once. At this time,
he decided to return to a lower elevation. After
walking 14 hours, he had descended to 6,500 feet
(2,000 M.). During the descent, he was extremely
weak and dyspneic. That night (the ninth on
the trail), he sat propped against a tree struggling for breath. Early the next morning he was
evacuated by helicopter to Fresno, California,
where he was admitted to a local hospital.
At the time of admission there the patient was
still in moderate respiratory distress with cyanosis
of the nailbeds and face. Numerous crepitant rales
were audible during inspiration over both lower
lung fields. The heart was normal in size and no
murmurs were heard. The pulmonic second sound
was widely split, more so during inspiration. The
remainder of the physical examination was within
normal limits.
Urinalysis, electrocardiogram, and routine examination of the blood were normal. Bilateral pulmonary densities, present on the admission chest
film, disappeared within a few days. Once again
the densities increased before they cleared (fig. 3).
Recovery was prompt and complete, following
Circulation, Volume XXV, June 1962
933
therapy consisting only of oxygen and bed rest.
He was discharged on the fifth hospital day and
has remained well since.
Case 2
W.B., a 46-year-old surgeon, arrived in good
health at Alta, Utah, on April 1, 1961. He had
traveled by air from his home at sea level. One
month before he had skied without difficulty at
Sun Valley, Idaho, (6,000 to 9,000 feet-1,800
to 2,750 M.).
At Alta he skied vigorously for 2 days in
heavy spring snow. On the evening of the second
day, he noticed nasal stuffiness. The next day
he experienced progressively increasing shortness
of breath, a cough productive of small amounts
of clear sputum, feverishness, and a severe headache. That evening he was barely able to climb
the stairs to his room because of weakness. He
was forced to remain in bed during the next
3 days because of dyspnea, cough, and weakness.
On the sixth day at Alta, the patient became
noticeably eyanotic. He was brought to Salt Lake
City and was immediately admitted to the hospital.
The headache disappeared on descent but cyanosis
persisted. At the onset of his illness, he had taken
two antibiotics orally without relief.
At the time of admission, the patient was
severely dyspneic and moderately eyanotic. The
temperature was 99.6 F. (orally), pulse 100 per
minute, respirations 28 per minute, and blood
pressure 140/90 mm. Hg. Breathing was labored
but excursion of the chest was equal bilaterally.
Percussion sounds were normal; however, tactile
fremitus was increased over the lower lobe of the
right lung. Fine and coarse rales were heard
over the entire right lung and lower lobe of the
left lung. There was no cardiomegaly. The heart
sounds were faint. The pulmonic second sound
was slightly louder than the aortic second sound
and was split throughout the respiratory cycle.
No murmurs were detected. The remainder of
the physical examination was within normal limits.
The volume of packed red cells was 42 ml./100
ml. on the day of admission and 48 ml./100 ml.
the following day. The white blood cell count was
8,200/mn.3 with 87 per cent neutrophils, 8 per
cent lymphocytes, 3 per cent monocytes, 1 per
cent basophils, and 1 per cent eosinophils. Several
electrocardiograms and urinalyses were normal.
Serial roentgenograms of the chest revealed a
normal heart shadow and extensive bilateral pulmonary infiltrations, which cleared rapidly (fig. 4).
The patient recovered promptly with administration of oxygen by nasal catheter and bed rest.
On the day after admission, the intensity of the
heart sounds had increased, a faint gallop rhythm
was noted over the right precordium, and the
FRED, SCHMI-DT, BATES, HECHT
93.1
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Figure 3
Serial roentgenogranms of the chest of patieWt T. B. Second4 episode. Note the iniereaise
in parenchymal lesions in the second roentgjenogramn.
pulhuionic sound had increased in intensity but
was no longer split. On the third day, physieal
exainination was; noirmal and the patient was
discharged essentially wvell.
Discussion
Episodes of acute pulmonary edemna of altitnde reported previously were the consequeniee of exposure to high altitude of aln
unacelimatized ildividual (or of one who had
.lost previous acclimatization). They were usu-
ally associated with severe physical exertion:.
(nountain climbiiig, skiing, runniincg, etc.).
The exact meehanisnms leading to the illness
have nlever been clearly defined btut left veuitricular failure or pulmonary infection have
leen inplicated' ,6 Intrinsic cardiac disease,
hlowvever, has been absenlt in almnost all the
eases reported to date. In no case has acute
lplllmlonlarY edemua of altitude been l)roved to
be the result of left ventricular failure. The
three episodes reported here provide furtlher
evidenice against the role of infectious disease
or of left ventricuilar failure in the pathogenesis of this syndrome, anid strongly support
the assumitptioni that the pulmonary abnormality represenits acute edema rather than inflamCirculation, V/olutme XXV, June 1962
935
ACUTE PULMONARY EDEMA OF ALTITTIJDE
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48-61
4-9-61
4-1061
4-14-61
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Figure 4
Se riotl ct utyenogrons of the chnest of potient TV. B.
inatory consolidattion. Houston' postulated
that cold environmentt might aeenituate t-he
developmient of aeutle pIlmIloniary edema of
altitude. The appearance of this illness in
patient T.B. anid othlers (lurinig the sumLmer
months2,2 Olhow-\Ter, suggests that low tenperature is pohab]y not a critical causative
a
3,
faotor.
The two separate attacks experienced by
.B. sugg;est that ani unusual predisposition
in a suseeptible individual miight lead to the
An indevelopment of thlis syndrome.2'
herited susc eptibility miay be presenit: simiilar
episodes have oecurred ini siblings2 and, in-
T
Circulation, Volume XXV. JIune 1962
deed, the available evidenee suggests that the
unexpected death of T.B.'s father may have
1)een caused by acute pulimoniary edema of
altitude.
It is evidenit fr-om the normal left atrial
jpressiire recorded in T.B. that the inereased
resistanice to blood flow mllust have been somewhere in the pulmoinary vascular bed. The
usual mechan-ism of pulmonary hypertension
is coonstrictioni of the pulmoniary arterioles.
This process, however, being proximal to the
capillary bed, wouild not explain the development of pulhnonary edemra, which was present
unequivocally oln clinical grounds. Thus, to
936
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be consistent with the occurrence of both pulmnonary hypertension and pulmonary edema,
the increased vascular resistance must have
been distal to the capillaries, presumably
somewhere in the venous bed. It is difficult
to measure accurately pressure in the pulmonary veins because of the obstruction to flow
caused by the relatively large catheter.
Nevertheless, the very slight difference between pulmonary vein and left atrial pressure
indicates that "sphincters" at the pulmonary
vein-left atrial junction described recently"
were not the cause of the vascular obstruction.
Therefore, one is forced to implicate the pulinonary venous capillaries or venules. The
relatively rapid development and clearing of
the illness, and particularly the dramatic
clinical and hemodynamic response to oxygen
inhalation (decrease in pulmonary artery
pressure and calculated pulmonary vascular
resistance) provide strong evidence that the
increased resistance (presumably venous) was
due to inereased vasomotor activity rather
than to an organic lesion. Transient pulmonary venoconstrietion has been produced experimentally in animals.7-10 Its contribution
to pulmonary edema in human subjects has
been postulated11 but to our knowledge adequate proof has not been presented before.
Both subjects showed transient clinical evidence of right ventricular overload. The pulmionary artery pressure was elevated in the
one instance in which it was measured. It
may have been even higher a-t the peak of
the illness. Pulmonary arteriolar resistance
could not be determined accurately because
of the ina,bility to obtain valid "wedge" pressures in spite of repeated adequate positioning
of the catheter. "Wedge" pressures, however,
could not have been less than 10 mm. Hg (pulpressure) or more than 40
mm. Hg (diastolic level of pulmonary artery
pressure). Since pulmonary edema, here presumably caused by pulmonary venous contriction, could not have occurred with venous
pressures of less than 25 mm. Hg, a value between 30 and 35 mm. Hg for the latter and
therefore for the "wedge" pressure cannot
monary venous
FRED, SCHMIDT, BATES, HECHT
be far off. The pulmonary arteriolar resistance index would then have measured between
4.0 and 5.5 clinical units, only slightly above
normal at the time these measurements were
made. Reduced oxygen tension, which in these
cases seems to have led to pulmonary venous
constriction, may simultaneously have exerted
an effect on the pulmonary arteriolar system
also; or the existence of pulmonary venous
congestion precipitated arteriolar constriction
in a manner as yet unknown.
At any rate, the onset of acute pulmonary
edema of altitude seems related to exposure
of a susceptible individual to a lowered oxygen tension in the inspired air. The abnormal
vascular response that follows is reversible by
the administration of oxygen and descent to
lower altitude. The use of digitalis or antibiotics is not likely to be beneficial.
Summary
Three separate episodes of acute pulmonary
edema are described that developed in two
otherwise healthy individuals during heavy
exertion at high altitudes. Detailed physical
examination and laboratory studies failed to
demonstrate pulmonary infection or cardiac
disease. Data obtained by cardiac catheterization during one of these episodes revealed
elevation of the pulmonary artery pressure
and a normal left atrial pressure.
This syndrome appears to be the consequence of pulmonary vascular obstruction
distal to the capillary bed, presumably in the
pulmonary veins. It is brought about by exposure of susceptible individuals to high
altitudes, and is completely reversed by oxygen administration.
Acknowledgment
Grateful acknowledgment is made to the two
physicians, T. B. and W. B., who are the subjects
of this report. Without their full cooperation and
assistance, these studies could not have been carried
out. Dr. A. Barker of Salt Lake City kindly allowed
us to study the second patient. Dr. Roger K. Larson
permitted the use of the observations made on the
first patient in Fresno, California. Drs. James M.
Rodda, Richard L. Murtland, and Russell Williams
of Monterey, California, aided in the study of T. B.
following his recovery from the first episode. Dr.
Circulation, Volume XXV, June 1962
937
ACUTE PULMONARY EDEMA OF ALTITUDE
Theofilos Tsagaris helped in the cardiac catheterization studies, and Dr. Hiroshi Kuida offered valuable
suggestions in the preparation of the manuseript.
8.
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T., TtNYI, M., SZUES, Zs.: The role of the
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Sydenham drew a sharp distinction between acute and chronic diseases. He saw
in disease, particularly in the acute forms, a sort of battle between the forces of Nature
resident in the patient's body and the noxious agents. These agents arise within the
body in consequence of faulty digestion or faulty mixture of the bodily juices. Diseases
are chronic because the reaction of the body against the harmful agent is slow in
developing, or because the agent continues to act over a long period of time. He lays
much stress on bodily disposition and age and sex and season and climate, and their
influence upon the course of disease. In these various respects Sydenham saw much
more deeply than his contemporaries. Sydenham's definition of disease shows a
truly remarkable insight. It is as follows: "An effort of Nature, striving with all her
might to restore the patient by elimination of the morbific matter."-DAVID RIESMAN,
M.D. Thomas Syndenham, Clinician. New York, Paul B. Hoeber, Inc., 1926, p. 24.
Circulation, Volume XXV, June 1962
Acute Pulmonary Edema of Altitude: Clinical and Physiologic Observations
HERBERT L. FRED, ALEXANDER M. SCHMIDT, TALCOTT BATES and HANS
H. HECHT
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Circulation. 1962;25:929-937
doi: 10.1161/01.CIR.25.6.929
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 1962 American Heart Association, Inc. All rights reserved.
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